非诺特罗对内毒素诱导的MyD88表达发挥抑制作用与抗炎效应相关  

Inhibition of LPS-induced expression of myeloid differentiation factor 88 by fenoterol is associated with its anti-inflammatory effect

作　　者：王伟[1] 胥婕[1] 贺蓓[2] 

机构地区：[1]北京大学第三医院感染疾病科,100191 [2]北京大学第三医院呼吸科,100191

出　　处：《实用医学杂志》2014年第18期2890-2893,共4页The Journal of Practical Medicine

摘　　要：目的:探讨β2肾上腺素受体激动剂非诺特罗(fenoterol)在单核细胞上抑制内毒素(lipopolysaccharide,LPS)诱导炎症的分子机制。方法:选择THP-1单核细胞系,ELISA(酶联免疫吸附剂测定)方法检测在有或无fenoterol预先干预下,LPS刺激的THP-1细胞上清中炎症因子肿瘤坏死因子-α(TNF-α)、单核细胞趋化蛋白-1(MCP-1)分泌及野生型和MyD88-/-(髓样分化因子,myeloid differentiation factor 88)小鼠腹腔巨噬细胞上清中炎症因子TNF-α、IL-1β(白介素-1β)分泌;western blot方法检测有或无fenoterol预先干预下,LPS刺激的MyD88表达。结果 :fenoterol可以显著抑制THP-1细胞上LPS诱导的MyD88的表达及TNF-α、MCP-1的分泌和小鼠巨噬细胞TNF-α、IL-1β的分泌,MyD88-/-小鼠腹腔巨噬细胞对LPS的反应显著低于野生型小鼠腹腔巨噬细胞。结论:MyD88在LPS诱导的炎症中发挥重要作用,fenoterol对LPS诱导的MyD88表达发挥抑制作用与其抗炎效应相关。ObJective To explore the molecular mechanism of inhibition of LPS-induced inflammation by fenoterol, a 132 adrenoceptor agonist in monocyte. Methods Concentrations of interleukin 1β（IL-1β）, tumor necrosis factor a （TNF-a） and MCP-1 from cell supernatants from THP-1 cells and wild type or MyD88-/- mice peritoneal macrophages stimulated by LPS in the presence or absence of fenoterol were determined by use of anELISA system. Expression of MyD88 （myeloid differentiation factor 88） stimulated by LPS in the presence or absence of fenoterol were determined by Western blot. Results Fenoterol inhibited LPS-induced activation of MyD88 and secretion of inflammatory cytokines （TNF-a, MCP-1, and IL-1β）. The reaction of MyD88-/- mice peritoneal macrophages to LPS was much lower than that of the wild type mice peritoneal macrophages. Conclusions MyD88 plays an important role in inflammation induced by LPS. The inhibition of LPS-induced expression of MyD88 by fenoterol is associated with its anti-inflammatory effect.

关 键 词：非诺精罗 单核细胞 LPS 抗炎 MYD88 

分 类 号：R363[医药卫生—病理学]